Translating developmental time across mammalian species

Clancy, Barbara; Darlington, Richard B.; Finlay, Barbara L.

doi:10.1016/s0306-4522(01)00171-3

Cited by 1,119 publications

(955 citation statements)

References 48 publications

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“…We include our novel "neuroinformatics" technique to the latter approach (Clancy et al, 2000;Clancy et al, 2001;Clancy et al, 2006;Finlay and Darlington, 1995), based on three related strengths: 1) acquisition and integration of large databases of multiple data types, 2) analyses using standard multivariate techniques made simpler by increased computing power, and 3) public availability through Web-based interfaces. These tools allow us to make accurate predictions of cross species developmental sequences based on multiple events in multiple species.…”

Section: Model Speciesmentioning

confidence: 99%

“…Additionally, the stage approach is based on somatic morphology, and presumes that brain development is linearly predictable from somatic development, and that all parts of the brain develop at equivalent rates. It is increasingly clear, however, that neural development detaches from somatic development to occur at a different pace in different species, and that brain regions detach from each other, compounding systematic comparison errors between somatic and brain development (Clancy et al, 2000;Clancy et al, 2001;Verley, 1977).…”

Section: Carnegie Stagesmentioning

confidence: 99%

“…Although the authors make no attempt to directly translate development across species, this study is an example of the manner with which the conservation of developmental sequences across species is presumed -the human study simply makes use of non-human data to "fill in" gaps. This assumption is possible because close similarities in the manner in which mammalian brains develop are well documented (Finlay and Darlington, 1995;Finlay et al, 2001;Finlay et al, 1998;Striedter, 1999;Striedter, 2005) and, when properly considered, can be used to equate developmental time across mammalian species with confidence (Clancy, 2006;Clancy et al, 2000;Clancy et al, 2001;Clancy et al, 2006;Verley, 1977). Some studies have been directly prompted by evolution-based questions.…”

Section: Evolutionary Event-based Comparisonsmentioning

confidence: 99%

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Extrapolating brain development from experimental species to humans

et al. 2007

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To better understand the neurotoxic effects of diverse hazards on the developing human nervous system, researchers and clinicians rely on data collected from a number of model species that develop and mature at varying rates. We review the methods commonly used to extrapolate the timing of brain development from experimental mammalian species to humans, including morphological comparisons, "rules of thumb" and "event-based" analyses. Most are unavoidably limited in range or detail, many are necessarily restricted to rat/human comparisons, and few can identify brain regions that develop at different rates. We suggest this issue is best addressed using "neuroinformatics", an analysis that combines neuroscience, evolutionary science, statistical modeling and computer science. A current use of this approach relates numeric values assigned to ten mammalian species and hundreds of empirically derived developing neural events, including specific evolutionary advances in primates. The result is an accessible, online resource (http:// www.translatingtime.net/) that can be used to equate dates in the neurodevelopmental literature across laboratory species to humans, predict neurodevelopmental events for which data are lacking in humans, and help to develop clinically relevant experimental models.

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Section: Model Speciesmentioning

confidence: 99%

Section: Carnegie Stagesmentioning

confidence: 99%

Section: Evolutionary Event-based Comparisonsmentioning

confidence: 99%

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Extrapolating brain development from experimental species to humans

et al. 2007

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“…This period corresponds to the first 2 weeks of postnatal life in the rat, in terms of similar neurodevelopmental changes (Bayer et al, 1993;Clancy et al, 2001). This means that treatment with drugs that inhibit the neurodevelopmental process should occur during these weeks in rats.…”

Section: Introductionmentioning

confidence: 96%

Spatial Memory Deficits Induced by Perinatal Treatment of Rats with PCP and Reversal Effect of D-Serine

Andersen

Pouzet

2004

Neuropsychopharmacol

119

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It has been suggested that perinatal treatment with the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist phencyclidine (PCP) induces transient neurodegeneration in the limbic and cortical structures of rats. Since dysfunction of these structures is associated with cognitive deficits in patients with schizophrenia, we studied the effects of subchronic treatment with PCP in perinatal rats with respect to spatial reference, reversal, and spatial working memories using the Morris water maze task in adulthood. In addition, we investigated the effect of D-serine, which has clinical relevance for the treatment of cognitive deficits in patients with schizophrenia. Our goal was to develop a neurodevelopmental model with predictive validity for the cognitive dysfunction described in patients with schizophrenia. Male and female Sprague-Dawley rats were treated with either saline or PCP (8.7 mg/kg s.c.) on days 7, 9, and 11, postnatal, and the long-term behavioral effects were investigated in adulthood. Male PCP-treated rats were slightly impaired during the spatial reference memory task, but strongly impaired during the reversal and spatial working memory tasks. Female rats were not significantly affected by this treatment. This cognitive deficit was reversed by chronic treatment with D-serine. We suggest that this model mimics some of the cognitive deficits of patients with schizophrenia and might be appropriate for the screening of putative antipsychotic agents for the treatment of these cognitive deficits.

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“…Exposure to propofol for 5 hour caused death of neurons and oligodendrocytes in foetal and neonatal NHP brain 6. However, little attention was paid to the early stage of gestation, which is equivalent to the early pregnancy of human 7. It is reported that 0.75% to 2% gestational women have to experience non‐obstetric surgery due to various medical problems 8.…”

Section: Introductionmentioning

confidence: 99%

Propofol exposure during early gestation impairs learning and memory in rat offspring by inhibiting the acetylation of histone

Lin

Wang

Feng

et al. 2018

J Cellular Molecular Medi

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Propofol is widely used in clinical practice, including non‐obstetric surgery in pregnant women. Previously, we found that propofol anaesthesia in maternal rats during the third trimester (E18) caused learning and memory impairment to the offspring rats, but how about the exposure during early pregnancy and the underlying mechanisms? Histone acetylation plays an important role in synaptic plasticity. In this study, propofol was administered to the pregnant rats in the early pregnancy (E7). The learning and memory function of the offspring were tested by Morris water maze (MWM) test on post‐natal day 30. Two hours before each MWM trial, histone deacetylase 2 (HDAC2) inhibitor, suberoylanilide hydroxamic acid (SAHA), Senegenin (SEN, traditional Chinese medicine), hippyragranin (HGN) antisense oligonucleotide (HGNA) or vehicle were given to the offspring. The protein levels of HDAC2, acetylated histone 3 (H3) and 4 (H4), cyclic adenosine monophosphate (cAMP) response element‐binding protein (CREB), N‐methyl‐D‐aspartate receptor (NMDAR) 2 subunit B (NR2B), HGN and synaptophysin in offspring's hippocampus were determined by Western blot or immunofluorescence test. It was discovered that infusion with propofol in maternal rats on E7 leads to impairment of learning and memory in offspring, increased the protein levels of HDAC2 and HGN, decreased the levels of acetylated H3 and H4 and phosphorylated CREB, NR2B and synaptophysin. HDAC2 inhibitor SAHA, Senegenin or HGN antisense oligonucleotide reversed all the changes. Thus, present results indicate exposure to propofol during the early gestation impairs offspring's learning and memory via inhibiting histone acetylation. SAHA, Senegenin and HGN antisense oligonucleotide might have therapeutic value for the adverse effect of propofol.

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Translating developmental time across mammalian species

Cited by 1,119 publications

References 48 publications

Extrapolating brain development from experimental species to humans

Extrapolating brain development from experimental species to humans

Spatial Memory Deficits Induced by Perinatal Treatment of Rats with PCP and Reversal Effect of D-Serine

Propofol exposure during early gestation impairs learning and memory in rat offspring by inhibiting the acetylation of histone

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